Phases of Cardiac Arrest

  1. Prearrest: Includes the patient's comorbidities and preexisting illnesses as well as the precipitating events (i.e. respiratory insufficiency). Often includes derangement in vital signs and physiological state. Rapid Response Teams and early warning systems (i.e. PEWS) developed to address this stage 
  2. Arrest: The period of time between actual arrest and onset of effective CPR. 
  3. Low flow (CPR): PALS/ACLS algorithms, pushing hard/fast, allowing full chest recoil between compressions, minimizing interruptions in compressions. 
  4. Postresuscitation: High risk period for further deterioration and period of identifying and managing ongoing precipitating factors


  • Estimated that 2-6% of children admitted to PICU and 4-6% admitted to pediatric cardiac units will suffer cardiac arrest1,2,3 
  • ~66% of in pediatric in hospital cardiac arrests achieve ROSC and more than 25% will survive to hospital discharge with ~75% of those having good neurologic function3
  • Out of hospital arrests have worse outcomes, with less than 30% of children receiving bystander CPR and often prolonged no-flow times. <10% survive the initial event and neurological injury is common


  1. Low Flow State (CPR)
    • CO and pulmonary blood flow much less than during normal sinus rhythm (~25%). Cerebral blood flow approximately 50% of normal
    • Avoid hyperventilation as it can lead to increased intrathoracic pressure and impair venous return
    • Nonetheless, as opposed to a code event that is cardiac (ie VT/VF) in nature, most pediatric arrests are respiratory in origin and hence, their initial PaO2 and PCO2 will likely be markedly abnormal, hence adequate ventilation and oxygenation is still crucial
    • Goal to provide adequate myocardial perfusion pressure (MPP) to regain ROSC. MPP= Aortic diastolic pressure - Right atrial pressure. It is during the recoil stage of compressions that RAP falls more than Aortic diastolic pressure, allowing blood to flow into the coronary arteries. Hence, devices such as the active compression device (attaches to anterior chest like a plunger and allows active decompression) may aid with restoring coronary perfusion
    • Compression/Ventilation ratio for 2 person CPR of 15:2 minimizes interruptions in CPR while also providing adequate ventilation
    • Epinephrine (high doses providing primarily alpha 1 effect causing increased PVR and SVR and improves MPP. Increases likelihood of successful defibrillation. Vasopressin has similar vasoconstricting effects except it does not increase PVR. Similar (or potentially worse) outcomes when compared to epinephrine
    • Calcium: in absence of clear clinical indication like hypocalcemia or hyperkalemia, no evidence to support use of calcium and potentially worse outcomes4 
    • Bicarbonate: Routine use not recommended as no evidence that it improves outcomes and some studies have shown worse outcomes even in the setting of severe metabolic acidosis5 Role if pacemaker present as acidosis can increase pacemaker thresholds, also indicated with TCA overdose, hyperkalemia, hypermagnesemia, or Na Channel blocker toxicity. Not sufficient evidence to recommend THAM
    • VF/VT estimated to occur at some point in 27% of in hospital pediatric cardiac arrests. Mortality directly related to delay in appropriate defibrillation (7-10% per minute). 2 J/kg defibrillation. More evidence to support use of amiodarone (5 mg/kg) than lidocaine for shock resistant VF/VT in adult patients
    • ETCO2 monitoring not currently routine but can demonstrate adequacy of compressions as with no pulmonary blood flow, your ETCO2 reading will be zero while with effective compressions, ETCO2 should rise (>15 mmHg)

    • Mild hypothermia (32-34 C) improves outcome in adult patients with out of hospital VF arrest 6,7
    • Neonatal trials have also shown improved outcomes with hypoxic-ischemic encephalopathy 8,9
    • Avoid hyperthermia. Ongoing trial (THAPCA, PI Dr. Frank Moler) investigating Therapeutic Hypothermia After Pediatric Cardiac Arrest in both in/out of hospital settings. The THAPCA Out of Hospital Trial did not show any significant differences in outcomes (mortality as well as recovery with near baseline cognitive ability-as measured by Vineland Adaptive Behavior Scales II) between therapeutic normothermia and therapeutic hypothermia. 
    • Avoid hyper/hypoglycemia
    • Post-arrest myocardial stunning similar to sepsis induced myocardial dysfunction

Extracorporeal Membrane Oxygenation Cardiopulmonary Resuscitation (ECPR)

  • VA ECMO is a viable option for rescue therapy, particularly with postoperative and potentially reversible myocardial dysfunction or refractory arrhythmias 
  • Requires significant institutional resources including adequate staffing, personnel, and equipment to be able to quickly mobilize 


1. A.D. Slonim, K.M. Patel, U.E. Ruttimann, M.M. Pollack:Cardiopulmonary resuscitation in pediatric intensive care units. Crit Care Med. 25 (12):1951-1955 1997 9403741
2. J.F. Rhodes, A.D. Blaufox, H.S. Seiden, et al.: Cardiac arrest in infants after congenital heart surgery. Circulation.100 (Suppl 19):194-199 1999
3. D.A. Parra, B.R. Totapally, E. Zahn, et al.: Outcome of cardiopulmonary resuscitation in a pediatric cardiac intensive care unit. Crit Care Med. 28 (9):3296-3300 200011008995
4. N. de Mos, R.R. van Litsenburg, B. McCrindle: Pediatric in-intensive-care-unit cardiac arrest: incidence, survival, and predictive factors. Crit Care Med. 34 (4):1209-12152006 16484906
5. K.L. Meert, A. Donaldson, V. Nadkarni, et al.:Multicenter cohort study of in-hospital pediatric cardiac arrest. Pediatr Crit Care Med. 10 (5):544-553 2009 19451846
6. Hypothermia after Cardiac Arrest Study Group: Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 346 (8):549-556 2002 11856793
7. S.A. Bernard, T.W. Gray, M.D. Buist, et al.: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 346 (8):557-563 200211856794
8. P.D. Gluckman, J.S. Wyatt, D. Azzopardi, et al.:Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet. 365 (9460):663-670 2005 15721471
9. S. Shankaran, A. Laptook, L.L. Wright, et al.: Whole-body hypothermia for neonatal encephalopathy: animal observations as a basis for a randomized, controlled pilot study in term infants. Pediatrics. 110 (2 Pt 1):377-3852002